Effect of miR-23 on Oxidant-Induced Injury in Human Retinal Pigment Epithelial Cells
Abstract
Purpose Micro(mi)RNAs negatively regulate a wide variety of genes through degradation or posttranslational inhibition of their target genes. The purpose of this study was to investigate the role of miR-23a in modulating RPE cell survival and gene expression in response to oxidative damage. Methods The expression level of miR-23a was measured in macular retinal pigment epithelial (RPE) cells of donor eyes with aged-related macular degeneration (AMD) and age-matched normal eyes by using qRT-PCR. Cultured human ARPE-19 cells were transfected with miR-23a mimic or inhibitor. Cell viability was assessed by the MTT assay. Apoptosis was determined by incubating cells with hydrogen peroxide (H(2)O(2)) or t-butylhydroperoxide (tBH). Caspase-3 activity and DNA fragmentation were measured by enzyme-linked immunosorbent assays. The protein relevant to apoptosis, such as Fas expression level, was analyzed by Western blot analysis. Results miR-23a expression was significantly downregulated in macular RPE cells from AMD eyes. H(2)O(2)-induced ARPE-19 cell death and apoptosis were increased by an miR-23a inhibitor and decreased by an miR-23a mimic. Computational analysis found a putative target site of miR-23a in the 3'UTR of Fas mRNA, which was verified by a luciferase reporter assay. Forced overexpression of miR-23a decreased H(2)O(2) or tBH-induced Fas upregulation, and this effect was blocked by downregulation of miR-23a. Conclusions The protection of RPE cells against oxidative damage i…
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Overexpression of miR-23a can decrease H2O2-induced ARPE-19 cell death and apoptosis by targeting Fas, protecting RPE cells against oxidative damage.
“The overexpression of miR-23a could decrease H2O2-induced ARPE-19 cell death and apoptosis by targeting Fas, thus achieving the purpose of protecting RPE cells against oxidative damage [51].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [51]
miR-23a is significantly reduced in human macular retinal pigment epithelial cells derived from age-related macular degeneration eyes.
“Additionally, miR-23a was significantly reduced in human macular retinal pigment epithelial (RPE) cells, which derived from age-related macular degeneration (AMD) eyes.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [51]
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MicroRNA-21 protects against the H2O2-induced injury on cardiac myocytes via its target gene PDCD4
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miRNAs as potential therapeutic targets for age-related macular degeneration
Wang, S., Koster, K. M., He, Y., & Zhou, Q. (2012) · Future Medicinal Chemistry · doi:10.4155/fmc.11.176 · Cited by 67 · see citing works
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Recent advances of miR-23 in human diseases and growth development
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- Authors
- Lin, H., Qian, J., Castillo, A. C., Long, B., Keyes, K. T., Chen, G., & Ye, Y.
- Affiliations
- From the Departments of Ophthalmology and Visual Sciences and
- Kunming Medical University (CN)
- The University of Texas Medical Branch at Galveston (US)
- Venue
- Investigative Opthalmology & Visual Science
- Published
- 2011-08-09
- Volume
- 52
- Issue
- 9
- Pages
- 6308
- ISSN
- 0146-0404 (ISSN-L)
- 1552-5783
- OpenAlex
- W2020203807
- Cited by
- 104
- References
- 2
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 5 · 2023: 3 · 2022: 6 · 2021: 12 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 11 · 2016: 7 · 2015: 9 · 2014: 9 · 2013: 10 · 2012: 9
- FWCI
- 8.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Investigative Ophthalmology & Visual Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Keywords
- miR-23a, retinal pigment epithelium, oxidative stress, apoptosis, Fas, hydrogen peroxide, tert-butyl hydroperoxide, microRNA regulation, 3' UTR target, ARPE-19 cells, caspase-3, retinal degeneration
- MeSH terms
- Aged, Aged, 80 and over, Cell Survival, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Humans, Hydrogen Peroxide, Macular Degeneration, Middle Aged, Mitochondria, Tissue Donors, Transfection, Blotting, Northern, Blotting, Western, Oxidants, Apoptosis, Oxidative Stress, fas Receptor, tert-Butylhydroperoxide, Reverse Transcriptase Polymerase Chain Reaction, MicroRNAs, Cytochromes c, Apoptosis Inducing Factor, Caspase 3, Retinal Pigment Epithelium
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